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Antimicrobial Agents and Chemotherapy, December 2001, p. 3504-3508, Vol. 45, No. 12
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.12.3504-3508.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Prevalence and Mechanisms of Macrolide Resistance in Invasive and Noninvasive Group B Streptococcus Isolates from Ontario, Canada

Joyce C. S. de Azavedo,1,2,* Mary McGavin,1,2,dagger Carla Duncan,1 Donald E. Low,1,2 and Allison McGeer1,2

Department of Microbiology, Toronto Medical Laboratories and Mount Sinai Hospital,1 and Department of Laboratory Medicine and Pathobiology, University of Toronto,2 Toronto, Canada

Received 23 March 2001/Returned for modification 23 June 2001/Accepted 22 September 2001

Macrolide resistance has been demonstrated in group B streptococcus (GBS), but there is limited information regarding mechanisms of resistance and their prevalence. We determined these in GBS obtained from neonatal blood cultures and vaginal swabs from pregnant women. Of 178 isolates from cases of neonatal GBS sepsis collected from 1995 to 1998, 8 and 4.5% were resistant to erythromycin and clindamycin, respectively, and one isolate showed intermediate penicillin resistance (MIC, 0.25 µg/ml). Of 101 consecutive vaginal or rectal/vaginal isolates collected in 1999, 18 and 8% were resistant to erythromycin and clindamycin, respectively. Tetracycline resistance was high (>80%) among both groups of isolates. Of 32 erythromycin-resistant isolates, 28 possessed the erm methylase gene (7 ermB and 21 ermTR/ermA) and 4 harbored the mefA gene; one isolate harbored both genes. One isolate which was susceptible to erythromycin but resistant to clindamycin (MIC, 4 µg/ml) was found to have the linB gene, previously identified only in Enterococcus faecium. The mreA gene was found in all the erythromycin-resistant strains as well as in 10 erythromycin-susceptible strains. The rate of erythromycin resistance increased from 5% in 1995-96 to 13% in 1998-99, which coincided with an increase in macrolide usage during that time.

* Corresponding author. Mailing address: Mount Sinai Hospital, 600 University Ave., Room 1483, Toronto ON M5G 1X5, Canada. Phone: (416) 586-8459. Fax: (416) 586-8746. E-mail: jdeazavedo{at}mtsinai.on.ca.

dagger Present address: The Samuel Lunenfeld Research Institute of Mount Sinai Hospital, Toronto ON M5G 1X5, Canada.

Antimicrobial Agents and Chemotherapy, December 2001, p. 3504-3508, Vol. 45, No. 12
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.12.3504-3508.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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